Neuromelanin (NM) accumulates in catecholamine long-lived brain neurons that are lost in neurodegenerative diseases. NM is a complex substance made of melanic, peptide and lipid components. NM formation is a natural protective process since toxic endogenous metabolites are removed during its formation and as it binds excess metals and xenobiotics. However, disturbances of NM synthesis and function could be toxic. Here, we review recent knowledge on NM formation, toxic mechanisms involving NM, go over NM binding substances and suggest experimental models that can help identifying xenobiotic modulators of NM formation or function. Given the high likelihood of a central NM role in age-related human neurodegenerative diseases such as Parkinson’s and Alzheimer’s, resembling such diseases using animal models that do not form NM to a high degree, e.g., mice or rats, may not be optimal. Rather, use of animal models (i.e., sheep and goats) that better resemble human brain aging in terms of NM formation, as well as using human NM forming stem cellbased in vitro (e.g., mid-brain organoids) models can be more suitable. Toxicants could also be identified during chemical synthesis of NM in the test tube.

In the present work, we describe the electrochemical behaviour of two opioids structurally related to aroyl amides of forensic interest, namely U-47700 and AH-7921. The data obtained allowed for the mise-au-point of a voltammetric determination protocol, that relies on differential pulse voltammetry (DPV) at a glassy carbon electrode in ethanol/0.1 M lithium perchlorate/0.10 M 2,6-lutidine. To apply the method to the analysis of real samples (urines), a clean-up and a preconcentration strategy by solid phase extraction (SPE) using the adsorbent Florisil have been developed. LOQ of 0.2 μg·mL⁻¹ in urine samples with an enrichment factor of 20 and linear range from 5 to 150 μg·mL⁻¹ were obtained.